The proposed study is designed to obtain a basic understanding of drugs that may act on GABA receptors in the mammalian central nervous system. Due to the complex nature of the synaptic connections within the central nervous system, studies involving an intact system are nearly impossible to interpret in terms of drug-receptor mechanisms at the cellular level. This problem has been overcome by the characterization of a mammalian GABA-receptor isolated on the soma of cat primary afferent neurons (Gallagher, Higashi and Nishi, 1974, 1975). Thus far, using standard electrophysiological techniques we have demonstrated that GABA produces a chloride dependent depolarization in the spinal cord, while others have suggested that GABA produces a chloride dependent hyperpolarization in the higher central nervous system. It is our hypothesis that a similiar GABA receptor may be present throughout the mammalian nervous system and the type of polarization is dependent upon the intracellular chloride concentration of the particular cell on which the GABA-receptor is located. An analysis of the mechanism(s) by which drugs may alter the GABA-receptor interaction at the cellular level in mammals has not been available. However, using electrophysiological techniques with the aid of differential interference microscopy at the GABA-receptor of the isolated cat spinal ganglion this type of analysis can be accomplished. Three groups of drugs will be used in this study: 1) anionic transport inhibitors; 2) anti-convulsants; and 3) psychoactive agents. Since GABA is an important veterbrate transmitter whose ionic mechanim of action involves an increased chloride permeability, and since GABA may be important in the genesis and/or treatment of certain disease conditions, these groups of drugs have been chosen to determine if their action at the cellular level may affect chloride permeability and thereby modulate the inhibitory action of GABA.